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SIU5 Neurology > Motor disorder > Flashcards

Motor disorder Flashcards

1
Q

the motor cortex is classified into 2 main pathways what are they?

A
  1. lateral pathway

2. ventralmedial pathway

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2
Q

describe the lateral pathway
what are the main tracts? (from where to where)
what role does it play in movement

A
  1. cortico-spinal tract (from cortex to SC)
  2. rubro-spinal tract (from red nucleues in midbrain to SC, more important in children as smaller pathway)
    Voluntary skilled movement by Direct cortical control
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3
Q

describe the ventro-medial motor pathway
what are the main tracts? (from which part of brain to where)
what role does it play in movement

A
  1. reticulospinal tract (from reticular nuclei in cerebellum in midbrain to SC) = postural control and reflex movement
  2. tectospinal tract (from superior colliculus in midbrain to SC, superior colliculus is higher up than medulla) = visual
  3. vestibulospinal tract (from vestibular nuclei in medulla in midbrain to SC) = auditory and balance
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4
Q

what is the overall effect of the lateral and ventro-medial pathways?

A

Coordinates the visual and auditory input w movement, direct you to turn around when you heard a sound/ react when see things

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5
Q

which two compotents are involved in the striatum part of the brain in the basal ganglia
why is it called striatum?

A

putamen and caudate nucleus

take away the top you see striation like tiger pattern

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6
Q

What is the basal ganglia consist of?

A

Striatum (putamen and caudate nucleus), external globus pallidus Gpe, internal globus pallidus Gpi, subthalamic nucleus STN, substantia nigra SN (zona compacta SNc and zona reticulata SNr
NOT thalamus!! (only receive output from basal ganglia)

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7
Q

why is substantia nigra important in parkinsons?

A

SN modifies the action/output from basal ganglia, this ability is lost in parkinsons

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8
Q

why is thalamus important in motor pathway?

A

receive output from basal ganglia and provide feedback pathway to the cortex, modulate the output from basal ganglia

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9
Q

Describe the brain region involved from deivision making, volition, planning to execution of an action

A

Cortex – prefrontal (making the decision), sensory (ventromedial pathway receive input), prefrontal cortex send signal to basal ganglia to thalamus (receive output and feedback to motor cortex, modulate CST output), basal ganglia send signal to red nucleus, reticular nuclei and superior colliculus and vestibular nuclei to give an action

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10
Q

Describe the stages of cortico-cerebellar connections. What is its purpose?

A

From sensory cortex down to cortico-ponto-cerebellar tract to the pontine nuclei then to the cerebellum cortex. The deep cerebellum nuclei send signal up to ventral thalamus via cerebellar feedback pathway- cerebellar-cortico tract. From thalamus to motor cortex. Down cortico-spinal tract to SC. The purpose includes motor learning and movement adjustment. Eg play a piano

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11
Q

What is Tourette’s syndrome? What went wrong in the basal ganglia? How can it be treated?

A

Rapid movement with stereotyped/ inappropriate sounds or speech. Inreased activity in NS pathway (high level of DA, increased output) treated w D2 rec-antagnoist (antipsychotic w s/e)

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12
Q

What does OCD stands for? Is it a disorder caused by abnormal basal ganglia? What treatment can be given?

A

Obsessive-compulsive disorder, it is caused by lesions in caudate/putamen in striatum which gives repetitive motor repsonse. Treated with SSRI (only treat change in mood not the cause)

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13
Q

prevelence of parkinsons

A

0.1% of population, disease of the elderly

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14
Q

What are the parkinsons symptoms?

A 
1 Bradykinesia – slow of movement 
2 Akinesia – absence/reduction of move, restlessness 
3 Rigidity
4 Tremor – pill rolling finger movement 
5 Poor balance 
6 Problem with initiating gait 
7 Speech problems – if speech muslce affected 
Progressive, Can cause depression
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15
Q

Describe the pathology of parkinsons in term of genetic

A

Genetic mutations of alpha-synuclein proteins which causes protein aggregation – forms insoluble lewy bodies –intracellularly inclusion of lewy bodies. Mutant parkin or ligase meaning ligase can no longer break down proteins, so prevents proteolysis. Oxidative stress from mito dysfunction. Overall causes (DA) cell death in (SNc of the) NS pathway

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16
Q

what is the knock-on consequences of SNc degeneration in parkinson?

A 
Loss of DA neurones - imbalance in direct and indirect pathways
increases activation of Gpi via indirect
Decreases inhibition via direct (Gpi)
Increases inhibition of thalamus
Switches off thalamo-cortical pathways
Loss of cortico-spinal output
Decreased movement, rigidity etc
17
Q

Treatement for parkinsons (outline 1st line)

brand name drugs?

A

1st line- oral L-DOPA (tyrosine hydroxylase is rate limiting, saturable conversion, so give L-DOPA can increase the DA level. It is converted to DA by DOPA-decarboxylase)
Combined use with peripheral decarboxylase inhibitors e.g. carbidopa, benserazide to reduce s/e
- madopar : cobenedopa (s/e constipation)
- sinemet : cocareldopa (Ldopa+ carbidopa)
- duoDopa : cont duodenal infusion of sinemet

18
Q

What are the downsides of L-DOPA

A

1 time limited. No long term benefit because parkinson is a progressive degeneration of neurone, run out of DA neuron to act on
2 Dsykinesias – like huntington
3 On-off syndrome
4 Nausea (DA in emetic centre)
5 Hypotension (DA on alpha1 rec, vasodilation)
6 Anorexia
7 Psychosis (DA on D2 rec mesolimbic pathway, increase +ve sym) pronography

19
Q

what are the other trt options for parkinsons?

A

DA receptor agonists: bromocriptine, pramipexole, apomorphine, rotigotine (inc patch) (s/e hallucination, sleepiness, impulsive)

retard degradation: COMT inhibitors - entacapone, MAO inhibitors - selegiline, rasagaline (s/e lesser hallucination)

DA release (increase): Amantadine – less effective than ldopa (less evidence)

Combination therapy with L-DOPA for max clinical benefit

20
Q

prevelence of huntington and age onset

A

Low incidence 0.01%- very low!

Appears between 30 and 50yrs

21
Q

relationship of motor and cognitive sym of huntingtons

A

Cognitive decline before motor

22
Q

sym of huntingtons

A 
Chorea - involuntary jerking
Grimacing (make faces)
Balance and gait (walking) problems
Cognitive decline, memory loss, depression
Swallowing and speech
Death 10-20 years following diagnosis
23
Q

What is the pathology of huntingtons?

A

Cell dealth in caudate/putamen–>impaired SN, striato-pallidal pathway but PRESERVED NS pathway (SNc is ok)
Hutington protein is normal in human body, but mutated huntington protein aggreagates and mirgrate from cytosol to nucleus and cause apoptosis. Also expanded repeats of codon for glutamine

24
Q

describe the Knock-on consequences of striatal degeneration

A 
Loss of caudate neurones 
decreased inhibition of GPe
increased inhibition of STN
Decreased excitation of GPi/SNc
Decreased inhibition of thalamus
Increased thalamo-cortical activity
Increase in cortico-spinal output
Hyperkinesia, facial tics etc
25
Q

trt for huntingtons

A

1 Baclofen (antispasticity) act at spinal level, Gaba b rec agonist on the spine
2 D2 antagonists (e.g. chlorpromazine)- antipsychotics, SE and unkown MOA
3 Treat symptoms e.g. (anti)depression
4 Neuroprotection- slow the degeneration
5 Caspase inhibitors - apoptosis??
6 Transplantation?
7 Stem cells?- limitation on what we can do

26
Q

Understand the underlying pathology that gives rise to PD

  • what is the purpose of DAnergic NS projection?
  • what went wrong?
A

THE EFFECT OF THE DOPAMINERGIC NIGROSTRIATAL PROJECTION IS TO INCREASE MOTOR ACTIVITY
in PD, Dysfunction in extrapyramidal system: basal ganglia –> Death of cells in substantia nigra (SNc). without Dopamine, you can’t ‘release the handbrake’

27
Q

describe the clinical features of PD

A 
Neurodegenerative, hypokinetic disorder
Key clinical motor symptoms/signs
1 Bradykinesia
2 +/- tremor
3 +/- rigidity 
4 +/- postural instability and gait disorder
Starts unilaterally
Very slowly progressive – years to decades
28
Q

Examination findings for PD

A 
1 paucity of movement 
2 stooped posture 
3 forward flexion (bending)
4 small shuffling steps 
5 difficulty initiate gait 
6 freeze 
7 decreased arm swing
29
Q

Drug Induced Parkinsonism

A

Drugs blocking D2 receptors in the striatum
Antipsychotics (D2 antag): TT Haloperidol
Anti emetics / prokinetics (D2 antag: Metoclopramide
Vestibular sedatives (BZs): Prochlorperazine (TT, 10x potent > chlorpromazine, D2 antag)
Sodium valproate (VNaC blocker)

30
Q

what is on-off flucturation?

A

An umbrella term for motor complications of advanced disease
Patients can fluctuate from off to on and vice versa
May be sudden or gradual
Due to changing levels of medication in the bloodstream, combined with cellular over-sensitivity

31
Q

what is on-off flucturation?

A

An umbrella term for motor complications of advanced disease, changing level of drug can affect pt sym from parkinson to huntingtons
May be sudden or gradual

32
Q

when does dyskinesia (huntington like) a s/e of parkinson med likely to occur

A

Occur when the medicine is working at its peak level, more in advanced parkinson due to narrowing of therapeutic window

33
Q

how to manage motor fluctuations

A

get a smooth conc profile- long acting preparations- decrease dosing interval (3x a day)
Advanced therapies- subcutaneous Apomorphine, Levodopa-Carbidopa Intestinal Gel (Duodopa), Deep Brain Stimulation

34
Q

ways of managing the PD inpatient as a pharmacist

A
  • ALWAYS GET MED ON TIME!!! (may be specific time)
  • NEVER stop med abruptly, w/d syn
  • neuroleptic malignant syndrome (due to DA blocking)
35
Q

consequences of stop parkinson med abruptively

A
  • rigidity
  • pneumonia
  • impaired swallow
  • pain
  • dsypnoea
36
Q

way of managing the peri-op patient

A
  • first on the list (first operation of the day in morn)
  • continue usual med w small amout of water
  • restart med immediately post op
  • seek advice if long surgery/ delirium
37
Q

Ways of managing the NBM parkinson patient

A
  • Use dispersible Madopar (cobenedopa) (same timings and dose)
  • can be Thickened reduce choking
  • Down nasogastric tube is ok
    If NO swallow: NG tube,
    Rotigotine (DA agonist) patch = ONLY NBM CHOICE
38
Q

what is the wearing off phase of parkinson med?

A

for over effective parkinson med, when the drug level drops, pt might not be able to move or swallow med

SIU5 Neurology (13 decks)

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